高压氧疗对脑损伤治疗作用机制的研究进展

Research Progress on the Mechanism of the HBOT Therapeutic Effect for the Brain Injury

脑损伤可引起脑组织的缺血缺氧。脑供血减少,会引起脑缺氧,但脑缺氧也可单独发生。若脑组织缺血缺氧的状态得不到及时纠正,氧参与的细胞内物质能量代谢将发生异常,如生成ATP的三羧酸循环、离子的转运等基本的生命活动都将受到影响,甚至停止。而蛋白质、核酸、脂质等物质的运输及代谢也将受到影响。这种状况持续数分钟,大脑的生理功能将受到影响,时间愈久这种变化愈难逆转。近年来,有研究表明,高压氧疗(HBOT)能改善损伤引起的脑组织缺血缺氧的状态,并对损伤的脑组织有修复的作用。其可能的途径如下:HBOT通过减少内皮素的生成,改善损伤后的脑血管痉挛状态、平衡脑血流以及降低升高的颅内压等,改善脑组织的缺血缺氧状态;并能通过改变MBP、caspases基因家族、Bcl-2/Bcl-xL以及TSPO、Nogo-A及其受体Ng-R等的表达,起到保护受损脑细胞、减少脑细胞凋亡以及促进神经细胞再生的作用;HBOT还可能通过增加胎盘生长因子(PLGF)的生成,起到促进血管生成及损伤脑组织再生的作用;此外,HBOT还能引起受损脑组织内多种炎症因子的改变,这也在一定程度上影响着脑损伤的预后。HBOT引起多种分子表达的改变,起到对损伤脑组织的修复作用,并进一步引起脑功能的改善,如认知能力、记忆能力以及日常交际和心理行为等方面的改善。以上都间接或直接地证明了HBOT对脑损伤的治疗作用。本文就HBOT对脑损伤治疗作用机制的研究进展加以综述。

Brain injury could lead to hypoxie-ischemic in the brain. Ischemia in brain always results in hypoxia, however, hypoxia can occur without ischemia. A prolonged hypoxie-ischemic in brain tissue will cause abnormalities of material and energy metabolism in brain cells. Furthermore, the basic life activities will be affected, for instance, TCA, which generates adenosine triphosphate （ATP） and the ion transporting, would even stop working. The metabolism of proteins, nucleic acids and lipid are also affected. In a few minutes,the physiological function of the brain will be seriously affected. The longer time this situation continues, the more difficult it would be to reverse the process. Recent studies show that HBOT can improve the condition of hypoxie-ischemic in brain and it can repair and regenerate the cerebral tissue to some extent. The mechanism may be as follows： firstly, it would reduce the ET level, and alleviate spasticity of blood vessels, for better balance of the blood flow and lowering the intracranial pressure in the brain, improving the condition of the hypoxie-ischemic in the brain. Secondly, HBOT can protect the brain against cell injury by increasing MBP, and against cell apoptosis by changing the expressions of caspases gene family, Bcl-2/Bcl-xL and TSPO, moreover, it can speed the neuron regeneration by decreasing the Nogo-A/Ng-R. Thirdly, HBOT can increase the PLGF generation, and in turn, the generation of vascular and help repair the injured brain tissue. Lastly, HBOT may alter the expressions of several cytokines, which may alleviate the conditions of brain injury patients. All of those may help the recovery of brain functions, including the cognitive, memory, communicative competence and mentality. These directly or indirectly show that HBOT is effective for treatment of the brain injury.